Turkish Journal of Hematology Volume: 35 - Issue: 4

Turk J Hematol 2018;35:300-314
LETTERS TO THE EDITOR
telangiectasia in a local community in the northern part of Japan. Hum
Mutat 2002;19:140-148.
3. Canzonieri C, Centenara L, Ornati F, Pagella F, Matti E, Alvisi C, Danesino
C, Perego M, Olivieri C. Endoscopic evaluation of gastrointestinal tract in
patients with hereditary hemorrhagic telangiectasia and correlation with
their genotypes. Genet Med 2014;16:3-10.
4. Grève E, Moussata D, Gaudin JL, Lapalus MG, Giraud S, Dupuis-Girod S,
Calender A, Plauchu H, Saurin JC. High diagnostic and clinical impact of
small-bowel capsule endoscopy in patients with hereditary hemorrhagic
telangiectasia with overt digestive bleeding and/or severe anemia.
Gastrointest Endosc 2010;71:760-767.
5. Chamberlain SM, Patel J, Carter Balart J, Gossage JR Jr, Sridhar S. Evaluation
of patients with hereditary hemorrhagic telangiectasia with video capsule
endoscopy: a single-center prospective study. Endoscopy 2007;39:516-520.
6. Ingrosso M, Sabbà C, Pisani A, Principi M, Gallitelli M, Cirulli A, Francavilla
A. Evidence of small-bowel involvement in hereditary hemorrhagic
telangiectasia: a capsule endoscopic study. Endoscopy 2004;36:1074-1079.
7. Holleran G, Hall B, Breslin N, McNamara D. Long-acting somatostatinanalogues
provide significant beneficial effect in patients with refractory
small bowel angioectasia: results from a proof of concept open label monocentre
trial. United European Gastroenterol J 2016;4:70-76.
8. Sauer H, Gunther J, Hescheler J, Wartenberg M. Thalidomide inhibits
angiogenesis in embryoid bodies by the generation of hydroxyl radicals. Am
J Pathol 2000;156:151-158.
9. Izquierdo Navarro Mdel C, Hernando Verdugo M, Cardaba Garcia E, Sanchez
Sanchez MT. Therapeutic failure with thalidomide in patients with recurrent
intestinal bleeding due to angiodysplasias. Farm Hosp 2016;40:230-232.
10. Palumbo A, Rajkumar SV, Dimopoulos MA, Richardson PG, San Miguel J,
Barlogie B, Harousseau J, Zonder JA, Cavo M, Zangari M, Attal M, Belch A,
Knop S, Joshua D, Sezer O, Ludwig H, Vesole D, Bladé J, Kyle R, Westin J,
Weber D, Bringhen S, Niesvizky R, Waage A, von Lilienfeld-Toal M, Lonial
S, Morgan GJ, Orlowski RZ, Shimizu K, Anderson KC, Boccadoro M, Durie
BG, Sonneveld P, Hussein MA; International Myeloma Working Group.
Prevention of thalidomide- and lenalidomide-associated thrombosis in
myeloma. Leukemia 2008;22:414-423.
©Copyright 2018 by Turkish Society of Hematology
Turkish Journal of Hematology, Published by Galenos Publishing House
Address for Correspondence/Yazışma Adresi: Stefania CHETCUTI ZAMMIT, M.D.,
Sheffield Teaching Hospitals, Royal Hallamshire Hospital, Academic Department of Gastroenterology,
Sheffield, England
E-mail : stf_che@yahoo.com ORCID-ID: orcid.org/0000-0002-1361-2204
Received/Geliş tarihi: July 21, 2018
Accepted/Kabul tarihi: July 23, 2018
DOI: 10.4274/tjh.2018.0253
Interleukin-2-330T/G and Interleukin-10-1082A/G Genetic
Polymorphisms and B-Cell Non-Hodgkin Lymphoma
İnterlökin-2-330T/G ve İnterlökin-10-1082A/G Genetik Polimorfizmi ve B-Hücreli Non-
Hodgkin Lenfoma
Beuy Joob 1 , Viroj Wiwanitkit 2
1Sanitation 1 Medical Academic Center, Bangkok, Thailand
2Honorary professor, Dr DY Patil University, Pune, India
To the Editor,
We read the publication “Association of Interleukin-2-330T/G
and Interleukin-10-1082A/G Genetic Polymorphisms with B-Cell
Non-Hodgkin Lymphoma (B-NHL) in a Cohort of Egyptians”
with great interest [1]. Abdel Rahman et al. [1] concluded
that “The present study highlights the possible involvement
of the [interleukin (IL)] IL-2-330T/G genetic polymorphism
in the susceptibility to [B-NHL] B-NHL in Egypt, especially
indolent subtypes. Moreover, IL-10-1082A/G is not a molecular
susceptibility marker for B-NHL in Egyptians” [1]. In fact, the
role of polymorphism of IL is widely mentioned in relationship
to NHL susceptibility [2]. We agree with the observation of
Abdel Rahman et al. [1]. The differences of the effects of IL-
2-330T/G and IL-10-1082A/G can be explained by molecular
quantum calculations of molecular weight changes. This is the
same phenomenon as seen in other polymorphisms and it can
affect the clinical appearance of many medical disorders, such
as the effect of CTLA-4 A49G polymorphism on autoimmune
blood disease [3]. For IL-2-330T/G and IL-10-1082A/G, the
change of molecular weight is equal to -107.07 and +16 per
molecule, respectively. This means that a molecule with IL-
2-330T/G requires more molecular mass and a molecule with
IL-10-1082A/G requires less molecular mass to complete a
biological process compared to a naïve molecule.
Keywords: Interleukin, Lymphoma, Polymorphism
Anahtar Sözcükler: İnterlökin, Lenfoma, Polimorfizm
Conflict of Interest: The authors of this paper have no conflicts
of interest, including specific financial interests, relationships,
301